The tear film, which is the interface between the external environment and the ocular surface has several different functions. It forms a smooth refractive surface over the otherwise irregular corneal surface and lubricates the eyelids. Moreover, it maintains an optimal extracellular environment for epithelial cells of the cornea and conjunctiva where the electrolyte composition, osmolarity, pH, oxygen and carbon dioxide concentrations, nutrient and growth factor concentrations are regulated within narrow limits.
Tears dilute and wash away noxious stimuli. They also provide an antibacterial system for the ocular surface and serve as an entry pathway for polymorphonuclear leukocytes in the case of injury to the ocular surface. As tears have many and varied functions, it is not surprising that they have a complex structure and are produced by several different sources.
The tear film consists of three layers. The inner layer is a mucous layer that coats the cornea and conjunctiva. It was previously thought to be 1 μm, but new evidence suggests that it may be far thicker. The mucous layer consists of mucins, electrolytes, water, IgA, enzymes, glycocalyx, microvilli, immunoglobins, and glycoproteins. The middle layer is an aqueous layer that is about 7 μm thick. This layer contains electrolytes, water, IgA, and proteins, many of which are antibacterial enzymes. Finally, the outer layer is a lipid layer about 0.1 μm thick, which floats on the aqueous layer. The lipid layer contains a complex mixture of hydrocarbons, squalene, wax esters, cholesterol esters, triglycerides, diglycerides, monoglycerides, free fatty acids, free cholesterol, phospholipid, sterol esters, and polar lipids.
Each layer of the tear film is secreted by a different set of orbital glands.
The lipid layer is secreted primarily by the meibomian glands located in the tarsal plates of the lower and upper lids. The glands lie in a row at the edge of the upper and lower eyelids and their ducts open directly onto the inner margin of the eyelids. There are approximately 30 to 40 meibomian glands in the upper lid and 20 to 30 smaller glands in the lower lid. Each gland has an orifice that opens on the lid margin between the tarsal “grey line” and the mucocutaneous junction. The sebaceous glands of Zeis, located at the palpebral margin of the tarsus, and the aprocine glands of Moll, located at the roots of each eyelash, also secrete lipid that is incorporated into the tear film.
Sebum, also called meibum, the meibomian gland secretion, increases the surface tension of the tear film and decreases its rate of evaporation. The evaporation rate of the normal tear film is low because of the protective lipid layer. Approximately 10% to 20% (0.085 μL/minute) of the total tears secreted are lost by evaporation. In the absence of the protective lipid layer, the rate of evaporation is increased 10 to 20 times (1.7 μL/minute).
Meibomian gland secretions contribute to the formation of a stable tear film. Meibomian gland dysfunction may result in dry eye syndrome, keratoconjunctivitis and contact lens intolerance, presumably due to an inadequate or a compromised tear film which is secondary to the meibomian gland dysfunction itself. Meibomian gland dysfunction may be often induced by soft contact lens wear, whilst mebomianitis may result from hard contact lens wear.
There are two major types of dry eye syndromes. Aqueous deficient dry eye syndrome is caused primarily from a lack of tear secretion from the lacrimal gland, whereas evaporative dry eye syndrome is typically caused by lipid insufficiency, a condition related to meibomian gland dysfunction. Both syndromes often co-exist.
It is thought that meibomian gland dysfunction may be caused in response to decreased androgen levels. Human lacrimal glands, meibomian glands and other ocular tissues have androgen receptors. The meibomian gland in particular appears to be a principal target site for androgen activity on the ocular substrate. Androgens appear to stimulate meibomian gland cells to produce lipids which maintains tear film stability and prevent tear film evaporation. Decreased androgen levels frequently occur with fluctuating hormonal changes associated with menopause, pregnancy, lactation and through the use of oral contraceptives. It is also associated with the ageing process in men and women. Auto immune diseases such as Sjörgen's syndrome, rheumatoid arthritis, diabetes, thyroid abnormality, asthma, cataracts, glaucoma and lupus appear to correlate with the presence of meibomian gland dysfunction and evaporative dry eye syndrome.
Certain medications such as antidepressants, decongestants, diuretics, ulcer medication, tranquillisers and beta blockers can also decrease the body's ability to produce lubricating lipids.
Use of antiandrogen medications for prostatic hypertrophy or cancer also appear to correlate with the incidence of meibomian glad dysfunction and evaporative dry eye syndrome.
Evaporative dry eye syndrome may also be caused by environmental conditions such as exposure to smoke, fluorescent lights, air pollution, wind, heaters, air conditioning and dry climates.
Similarly, behavioural patterns, particularly the tendency for VDU users to ignore the normal blinking process, may also interrupt tear production.
Contact lens wearers appear to be particularly susceptible to evaporative dry eye syndrome. Contemporary contact lenses are of two primary types: rigid gas permeable lenses (hard) and hydrogel lenses (soft) comprising between 30% to over 85% water of hydration. Rigid gas permeable lenses are commonly formed from a co-polymer of methylmethacrylate and silicon, termed siloxaneacrylate.
The tear film thickness on the eye is reported to be up to 10 microns, decreasing to 4.5 microns between blinks. The tear film is relatively thin when compared with the thickness of any contact lens, which varies from a minimum of 30 microns to an average of 60–120 microns, and over 250 microns for lenses of considerable optical power. Thus, the sheer mass of any contact lens may compromise the specific functions of the tear film which include the flushing action, the prevention of desiccation of the ocular tissue, the lubrication of the ocular and palpebral surfaces, the formation of an optically smooth curved surface, a vehicle for oxygen and carbon dioxide transport, and the defence of the cornea against trauma, infection or disease. The role of the lipid layer in preventing evaporation is relevant to contact lens wear. If the meibomian glands are obstructed, essentially eliminating the lipid layer, the rate of evaporation dramatically increases by a factor of 10 to 20.
The lipid layer on the surface of all contact lenses is compromised as compared to the lipid layer of the cornea without the contact lenses. A well-fitted contact lens has to rest on a continuous aqueous tear layer sandwiched between the lens and the epithelium, and it has to be coated with a continuous tear film complete with a superficial lipid layer. However, all contemporary contact lenses are unable to mimic the ocular surface properties, and therefore a comparable tear film on the lens surfaces is unable to form.
A lipid layer does not form on hard lenses. There are conflicting reports regarding the presence and/or characteristics of the lipid layer forming on soft lenses. Some claim the complete absence of a lipid layer, while others report it as present but thin, its depth being dependent on the water content of the lens.
Clinical experience indicates that individuals without objective signs of dry eyes or subjective symptoms may experience classical dry eye symptoms while wearing contact lenses. When the contact lens is placed on the eye, the lens alters the normal structure of the tear film and affects its rate of evaporation. It is thought that the lipid layer is compromised causing dehydration of the aqueous layer to accelerate and tears to macerate the skin.
The present invention seeks to overcome at least some of the aforementioned disadvantages